Navegando por Orientadores "YAMADA, Elizabeth Sumi"

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Ajustes posturais antecipatórios e compensatórios em idosos com e sem lombalgia
(Universidade Federal do Pará, 2021-03) GARCEZ, Daniela Rosa; CALLEGARI, Bianca; http://lattes.cnpq.br/0881363487176703; https://orcid.org/0000-0001-9151-3896; YAMADA, Elizabeth Sumi; http://lattes.cnpq.br/7240314827308306
Chronic low back pain (DLC) is associated with changes in postural control and is highly prevalent in the elderly. Research shows that aging and DLC are described as important factors that affect postural control. The postural control impairments increase the risk of falls. Researches evaluating the postural control in elderly people with DLC are still necessary for greater effectiveness in balance rehabilitation programs to prevention falls in this population. The objective of this study is to verify whether anticipatory postural adjustments (APAs) and compensatory postural adjustments (CPAs) are affected by DLC in elderly people by assessing their postural control during a self-initiated perturbation paradigm induced by rapid upper arm movement when pointing to a target. Elderly people were divided into: Group with DLC (GDLC) (n = 15) and Control Group (CG) (n = 15). The participants’ lower limb muscle onset and center of pressure (COP) displacements were assessed prior to perturbation and throughout the entire movement. T0 moment (i.e., the beginning of the movement) was defined as the anterior deltoid (DEL) onset, and all parameters were calculated with respect to it. The rectus femoris (RT), semitendinosus (ST), and soleous (SOL) showed delayed onset in the GDLC group compared with the control group: RF (control: -0.094 ± 0.017 s; GDLC: -0.026 ± 0.012 s, t = 12, p < 0.0001); ST (control: - 0.093 ± 0.013 s; GDL: -0.018 ± 0.019 s, t = 12, p < 0.0001); and SOL (control: -0.086± 0.018 s; GDL: -0.029 ± 0.015 s, t = 8.98, p < 0.0001). In addition, COP displacement was delayed in the GDLC group (control: -0.035 ± 0.021 s; GDL: -0.015 ± 0.009 s, t = 3; p = 0.003) and presented a smaller amplitude during APA COPAPA [control: 0.444 cm (0.187; 0.648); GDLC: 0.228 cm (0.096; 0.310), U = 53, p = 0.012]. The GDLC group required a longer time to reach the maximum displacement after the perturbation (control: 0.211 ± 0.047 s; GDLC 0.296 ± 0.078 s, t = 3.582, p = 0.0013). This indicates that GDLC elderly patients have impairments to recover their postural control and less efficient anticipatory adjustments during the compensatory phase. Our results suggest that people with GDL have altered feedforward hip and ankle muscle control, as shown from the SOL, ST, and RT muscle onset. This study is the first study in the field of aging that investigates the postural adjustments of an elderly population with GDLC. Clinical assessment of this population should consider postural stability as part of a rehabilitation program.
Acesso aberto (Open Access)
Análise comportamental e histológica de um modelo animal da doença de Parkinson em camundongos suíços
(Universidade Federal do Pará, 2011-12-29) GARCEZ, Daniela Rosa; YAMADA, Elizabeth Sumi; http://lattes.cnpq.br/7240314827308306
Parkinson’s disease (PD) is one of the most common aging-related neurodegenerative diseases, having a clinical presentation featuring classic motor symptoms related to the degeneration of dopaminergic neurons of the substantia nigra pars compacta (SNpc) and dopamine decr ease in the striatum. Animal models of PD are important tools employed by researcher aiming a better understading of pathophysiologic disease mechanisms and for evaluation of potential therapeutic interventions. Such models must mimic some aspect of the disease as for instances, the degeneration of nigral dopaminergic neurons. In this context, the PD model induced by the injection of the neurotoxina 6-hydroxydopamine (6-OHDA) has been widely established in rats but a better characterization in diferent mice strain is lacking, concerning both behavioral changes and the lesion in nigrostriatal system. Such characterization is important so that this model can be reliably used for investigations of therapeutic interventions. The goal of the present study was to improve the characterization of the unilateral 6-OHDA PD model using Swiss mice, through the evaluation of behavioral changes and the effects on the SNpc dopaminergic neurons. In this investigation we have used a single unilateral intraestriatal injection of 6-OHDA, in two different toxin concentrations: 10 µg/2µl e 20 µg/2 µl. Our results have demonstrated that both 6-OHDA concentrations used provoked severe loss of nigral dopaminergic neurons, amounting to 74,5% e 89,5% respectively. This neuronal loss was highly correlated to the apomorphine-induced rotational behavior but not to the ambulation assessed in the open field test. Therefore, intraestriatal injection of 10 µg/2µl or 20 µg/2µl of 6-OHDA, using Swiss mice, reproduce an effective unilateral 6-OHDA PD model that can be reliably employed in experiments aiming to investigate neuroprotective, cellular and/or pharmacological therapies for PD.
Acesso aberto (Open Access)
Avaliação da qualidade de vida de pacientes com Diabetes Mellitus tipo 1: dados do primeiro estudo multicêntrico no Brasil
(Universidade Federal do Pará, 2013) SOUZA, Ana Carolina Contente Braga de; FELÍCIO, João Soares; YAMADA, Elizabeth Sumi; http://lattes.cnpq.br/8482132737976863; http://lattes.cnpq.br/7240314827308306
The type 1 diabetes mellitus type 1 (T1DM) is the most common endocrine disease of childhood and adolescence and it negatively impacts the quality of life (QOL). The EuroQol is an instrument that assess the health state. It has been used in most global multicenter studies in diabetes and it has been shown to be an extremely useful and reliable tool. The aim of this study is to evaluate the QOL of patients with T1DM in Brazil, a country of continental proportions, by analyzing the EuroQol. For this purpose, we performed a retrospective and cross-sectional study, which analyzed questionnaires from patients with T1DM, answered in the period of December 2008 to December 2010 in 28 research centers in 20 cities of the four regions (Southeast, North-Northeast, South and Midwest). We also collected data about chronic micro and macrovascular complications and lipid profile. The assessment of quality of life by EuroQol shows that the average score assigned to general health is markedly lower than those found in two other T1DM population studies conducted in Europe (EQ – VAS from Germany, Netherlands and Brazil were 82.1 ± 14, 81 ± 15 and 72 ± 22, respectively). The EuroQol shows that the North-Northeast region has the best index in the assessment of the overall health status compared to the Southeast and lower frequency of self-reported anxiety -depression, compared to other regions of the country (North-Northeast = 1.53 ± 0.6, Southeast = 1.65 ± 0.7, South = 1.72 ± 0.7 and Midwest = 1.67 ± 0.7, p <0.05). Additionally, several known variables (age, duration of diabetes, physical activity, HbA1c, fasting glucose, and presence of chronic complications correlated with QOL (r = -0.1, p <0.05, r = -0.1, p <0.05, r = -0.1, p <0.05, r = -0.2, p <0.05, r = -0.1, p <0.05 and r = -0.1, p <0.05, respectively). This is the first population study to evaluate the quality of life of patients with type 1 diabetes in the south hemisphere. Our data indicates poorer quality of life of patients with T1DM in Brazil when compared to data from European countries. Although we found an inferior diabetes duration and lower presence of microvascular complications in the North -Northeast region compared to other regions, our data suggests the existence of additional factors responsible for better QOL and lower presence of anxiety-depression found in this region. More studies are necessary to identify these possible factors.
Acesso aberto (Open Access)
Avaliação do potencial neuroprotetor do beta-cariofileno em modelo murino de Doença de Parkinson induzido por 6-Hidroxidopamina
(Universidade Federal do Pará, 2019-06) AMARAL, Anderson Valente; YAMADA, Elizabeth Sumi; http://lattes.cnpq.br/7240314827308306
Parkinson’s disease (PD) is classified as a motor disturbance characterized by resting tremor, muscular rigidity, postural instability and bradykinesia. These symptoms are caused by progressive loss of dopaminergic neurons in the substantia nigra pars compacta (SNpc) and consequently depletion of dopamine on striatum (STR). The search for new therapeutical approaches that may delay or interrupt the neurodegeneration in PD is essential to promote a better quality of life for patients. Thus, we investigated whether beta-caryophyllene (BCP) has neuroprotective effects in the 6-OHDA murine model of PD. Then, we performed behavioral tests such as apomorphine-induced rotations and exploration in the open field, we measured the optical density from STR fibers, quantified neurons and microglia in the SNpc through stereology and evaluated the total antioxidant capacity from STR and midbrain. Our evidence demonstrates that BCP reduced the degree of neurodegeneration induced by 6-OHDA, improved motor performance, protected striatal dopaminergic fibers, protected dopaminergic neurons and reduced microglial activation in the SNpc. But did not alter the antioxidant capacity in the STR and midbrain. Hence, BCP treatment has a potential neuroprotective effect in this mouse model of PD, which deserves to be better characterized for translational application.
Acesso aberto (Open Access)
Avaliação in vitro do efeito genotóxico e neurotóxico da rotenona em populações neuronais de encéfalo de ratos
(Universidade Federal do Pará, 2011-12-28) LIMA, Geovanny Braga; YAMADA, Elizabeth Sumi; http://lattes.cnpq.br/7240314827308306
Parkinson’s disease is a neurogenerative disease that affects dopaminergic neurons of the substantia nigra whose neurons Project to the striatum. Rotenone is a compound widely used as pesticide and which has been implicated among the environmental factors that increase the risk of developing PD. An essay that evaluate DNA damage, such as the eletroforesis comet essay, was introduced in the present work, to better understand the neurotoxic effects of the rotenone in a experimental model of PD. The comet assay was applied to neurons from mixed mesencephalic cultures exposed to different concentrations of rotenone in two different exposure times, 24 and 48 hours. The mean comet damage index showed a significant difference between the control condition and all the rotenone concentrations tested in both exposure times. However, in the comparative analysis considering time exposure for equivalent concentrations, there was significant difference only with 20 and 30 nM rotenone concentrations. This study demonstrated that, in the experimental conditions used, the comet assay detected damage to the genetic material without detectable alterations in the MTT viability test (5 nM rotenone, 24h), suggesting that genotoxic alterations may precede viability alterations in rotenone-exposed neurons. It is not possible, however, to assure that such alterations are irreversible or not.
Acesso aberto (Open Access)
Investigação dos efeitos protetores do selenito de sódio sobre a neurotoxicidade do metilmercúrio em diferentes períodos de desenvolvimento de ratos wistar
(Universidade Federal do Pará, 2011-12-28) SANTOS, Nilton Barreto dos; COSTA, Edmar Tavares da; http://lattes.cnpq.br/6776869402973569; YAMADA, Elizabeth Sumi; http://lattes.cnpq.br/7240314827308306
Exposure to mercury compounds results in oxidative damages, seriously affecting the central nervous system both in humans and in experimental models. We used Wistar rats at different stages of neuro-development in order to investigate potential protective effects of selenium (sodium selenite) in an in vivo model of exposure to methylmercury (MeHg). Subjects (age groups P1 and P21) were given lactational and orally, respectively: vehicle, Selenium (5ppm), MeHg (10 ppm) or selenium (5 ppm) plus MeHg (10 ppm) for 20 and 10 days respectively (n = 8 per group). After treatment, the rats were submitted to the following behavioral tests: open field and Morris water maze to examine motor deficits and memory/learning, respectively. After intracardiac perfusion we performed immunohistochemistry for Neu-N. In order to evaluate possible deleterious effects in neuronal populations, we counted neurons in the hippocampus (polymorphic layer). As a result, we found significant reduction in locomotor activity of neonates (P1) when exposed to MeHg. Besides, groups exposed to MeHg (alone or in association with selenium) showed learning/memory deficits. P21 animals treated with MeHg showed increase in locomotor activity, effect abolished by concomitant administration of selenium. When submitted to water maze, only subjects in the control and selenium groups showed reduction of the time latency. As assessed by stereological counting, we noticed reduction in the number of hippocampal neurons only in P21 animals exposed to MeHg. Combined, our results showed that MeHg exposure produces age-dependent behavioral effects. Also, despite other findings in the literature, under our experimental conditions administration of selenium was only able to interfere with motor deficits in older animals, besides not being able to interfere with memory/learning deficits nor the MeHg-induced neuronal death. Possible mechanisms associated with these partial protective properties of selenium in the later stages of neural development have yet to be elucidated.
Acesso aberto (Open Access)
Modelo de doença de parkinson em camundongos baseado na injeção unilateral 6-hidroxidopamina no estriado: caracterização do curso temporal das alterações comportamentais e da degeneração nigroestriatal
(Universidade Federal do Pará, 2008-07-03) CARDOSO, Váldina Solimar Lopes; YAMADA, Elizabeth Sumi; http://lattes.cnpq.br/7240314827308306
Parkinson‘s disease (PD) is a common neurodegenerative disease that affects mainly elderly people. It is characterized by the progressive cell death of dopaminergic neurons in the nigrostriatal system, which causes the development of the classic tetrad of symptoms: resting tremor, muscular rigidity, bradikynesia and postural instability. There is evidence that both genetic and environmental factors play a role in the development of the disease. In order to better understand the mechanisms undelying this disease, several animal models have been used to mimic some aspect of the dopaminergic degeneration. The intracerebral injection of 6-OHDA has been one of the most used PD model. This toxin is preferentially injected into the striatum or in the substantia nigra to provoke a selective degeneration of dopaminergic neurons from the nigrostriatal pathway. When a unilateral injection is used, the animals display a stereotypical rotational behavior after pharmacological induction, and such behavior has been largely used as a measure of the degree of nigroestriatal degeneration. This model is well characterized in rats and has been an useful tool to test neuroprotective therapies. Mice, as much as rats, are also largely used in studies of DP, but the 6-OHDA model has not been well described. The objective of the present work was to improve the characterization of the hemiparkinsonism model based on a single unilateral intraestriatal injection of 6-OHDA in C57BL6 mice, to provide a more detailed evaluation of the temporal course of the neuronal dopaminergic degeneration in the substantia nigra and to establish the degree of correlation between the degeneration and behavioral changes. Our results showed that a single injection of 10 μg of 6-OHDA into the striatum causes progressive degeneration of nigral dopaminergic neurons dependent of survival time, and that there is a high correlation between the rate of degeneration and the rotational behavior induced by apomorphine. Spontaneous motor behaviors such as ambulation and rearing had a lower correlation with the degeneration. Therefore, we suggest that the rotational behavior induced by apomorphine provides a good measure of the degree of asymmetry in the nigrostriatal pathway of mice with 6- OHDA-induced hemiparkinsonism and that it can indeed be an useful tool in experiments to test therapies with neuroprotective potential for Parkinson’s disease.
Acesso aberto (Open Access)
Modelo in vitro de parkinsonismo experimental induzido por rotenona: investigação de mecanismos de ação, neuroproteção e morte celular
(Universidade Federal do Pará, 2011-12-29) MARTINS FILHO, Arnaldo Jorge; COSTA, Edmar Tavares da; http://lattes.cnpq.br/6776869402973569; YAMADA, Elizabeth Sumi; http://lattes.cnpq.br/7240314827308306
Increasing evidence has suggested a role for environmental factors, such as exposure to pesticides, in the pathogenesis of Parkinson’s disease. In experimental animals the exposure to rotenone, a common herbicide and piscicide, induces features of parkinsonism by inhibiting the activity of mitochondrial complex I. Here we propose to investigate rotenone-induced death of neurons by using primary neuron-enriched and neuron-glia cultures from the rat hippocampus and ventral mesencephalon. The neuronal loss was evaluated with the colorimetric MTT assay. Our results showed significant reduction in the cell viability after exposure to rotenone in a dose- but not in a timedependent manner. We also discovered a remarkable feature of rotenone-induced degeneration of cultured neurons. The higher susceptibility was observed in neuron-glia cultures from the ventral mesencephalon, suggesting that the presence of glia, especially microglia, is an important factor contributing to neurodegeneration. Also, as showed by immunohistochemistry, this type of culture presented the higher density of tirosinahidroxilase (TH)-positive neurons. Mechanistically, our results with calcium blockers showed a minimal role played by external calcium, and an important synergistic influence of the ions from the internal stores in the rotenone-induced neurodegeneration. Indeed, in this study, we report that aqueous extract of mahogany leaves didn’t protect against the rotenone-induced toxicity, in the used concentration; and promoted a synergistic effect when associated with rotenona. Finally, the mahogany leaves extract induced celular death both necrosis and apoptosis. The results of this study should advance our understanding of the mechanism of action for environmental factors in the pathogenesis of Parkinson’s disease.
Acesso aberto (Open Access)
Polimorfismos gênicos do tipo indel: o papel da vulnerabilidade genética no desenvolvimento da neuroinflamação e na fisiopatologia do Transtorno Depressivo Maior
(Universidade Federal do Pará, 2017-07-26) REIS, Deyvson Diego de Lima; BURBANO, Rommel Mario Rodriguéz; http://lattes.cnpq.br/4362051219348099; YAMADA, Elizabeth Sumi; http://lattes.cnpq.br/7240314827308306
The pathophysiology of depression still remains not fully understood. And despite the contributions of the monoaminergic hypothesis to the understanding of neurobiological aspects of this disorder, studies have been carried out to investigate the role of neuroinflammation, polymorphisms in genes that influence inflammatory activity and monoaminergic receptor functions in the development of major depressive disorder (MDD). However, few studies have analyzed the role of upstream inflammatory pathways (such as the role of NFKB1 and PAR1 genes, which are capable of influencing transcription of proinflammatory cytokines) and of the alpha 2 adrenergic receptor encoding gene's polymorphism (ADRA2B gene) in individuals diagnosed with depression. Therefore, the objective of this study was to analyze the role of the INDEL type polymorphisms of NFKB1 (rs28362491), PAR1 (rs11267092) e ADRA2B (rs34667759) genes in the development of major depressive disorder. Twelve patients diagnosed with MDD and 145 healthy controls had blood samples collected and the INDEL polymorphisms of these 3 genes were genotyped by a single multiplex reaction. The multiplex PCR products were separated by capillary electrophoresis and the data analyzed in GeneMapper 3.7 software (Applied Biosystems). This research found a statistically significant association between depression and Del/Del genotype of the ADRA2B gene (p = 0.002): these individuals presented a 6.41 times greater chance of developing depression when compared to Del/Ins and Ins/Ins genotypes. There was no statistical significance between the INDEL polymorphisms of NFKB1 and PAR1 genes and depressive phenotype. Our results suggest that the INDEL marker of the ADRA2B gene (rs34667759), specifically the deletion allele, is a possible genetic biomarker of vulnerability for the development of MDD.
Acesso aberto (Open Access)
Viabilidade e eficácia da telerreabilitação e da cartilha de exercícios para pessoas com doença de Parkinson residentes em uma região da Amazônia brasileira: um ensaio clínico randomizado
(Universidade Federal do Pará, 2023-12) RAMOS, Luciana Fernandes Pastana; YAMADA, Elizabeth Sumi; http://lattes.cnpq.br/7240314827308306; LOBATO, Bruno Lopes Santos
Parkinson's disease (PD) is a chronic and progressive neurodegenerative disorder, and the current treatment involves pharmacological intervention and physiotherapy. Telerehabilitation, which involves remote support and guidance for patients undergoing rehabilitation, can potentially improve access to physiotherapy services for people with Parkinson's disease, especially those who face geographic barriers to healthcare. The primary aim of this study was to assess the feasibility and efficacy of a telerehabilitation program for people with Parkinson's disease living in an underrepresented community of the Brazilian Amazon. We conducted a parallel-group, single-center, single-blind, randomized clinical trial involving 19 participants diagnosed with Parkinson's disease from Belém, Brazil. Participants were assigned to a 4-week individual telerehabilitation program or a booklet-based exercise program (control group). Assessments were conducted before the intervention, immediately after the intervention, and 4 weeks after the end of the intervention. We showed that our telerehabilitation program had high adherence among patients, with minimal adverse effects. Both telerehabilitation and booklet orientation reduced the time to complete the Timed Up and Go test. In conclusion, our telerehabilitation or booklet-based exercise program was feasible and effective for people with Parkinson's disease in an Amazonian setting. This trial was registered at the Registro Brasileiro de Ensaios Clínicos (ReBEC) under the identifier: RBR-6sz837s.